The standard therapy for treating colorectal cancer patients has been performed, typically, with chemotherapy using fluoropyrimidine-based antitumor agent (e.g., a combination of 5-fluorouracil (5-FU) and leucovorin (LV)), and optionally, with multidrug chemotherapy (FOLFIRI, FOLFOX, or the like) that additionally uses irinotecan or oxaliplatin. Such methods have achieved a certain therapeutic effect (Non-Patent Document 1).
However, when a colorectal cancer patient becomes refractory or intolerant to these standard therapies using 5-FU, irinotecan, or oxaliplatin, the choice of antitumor agent that can significantly prolong their survival is very limited. Further, although cetuximab, which is a chimeric antibody targeting the epithelial growth factor receptor (EGFR), and panitumumab, which is a fully human monoclonal antibody, are often selected for such colorectal cancer patients who are refractory or intolerant to standard therapy, it has been reported that these antitumor agents had no effects when the patients have colorectal cancer with KRAS gene mutation (Non-Patent Documents 2 and 3).
As explained above, despite the vigorous development of chemotherapies for colorectal cancer patients, their therapeutic effects are still insufficient. In particular, effective chemotherapies have not substantially been established for colorectal cancer patients with KRAS gene mutation. Further, since the effects of chemotherapies greatly depend on the genetic factors of the patients, there is no way to estimate the effects of the antitumor agents before the actual administration.